CHRISTCHURCH, New Zealand—Twenty-three percent of renal transplant recipients reported at least one attack of gout posttransplant, and two thirds of those patients had no gout prior to transplant, according to a new case-control study from researchers in New Zealand. Lisa Stamp, MD, with the department of medicine at Christchurch School of Medicine and Health Sciences, and colleagues also report that even among renal transplant recipients who suffered repeated episodes of gout, only 52% received a hypouricemic agent. Those who developed gout posttransplant were also twice as likely to be taking a loop diuretic.¹

"Once gout occurs posttransplant it tends to be recurrent and can have a significant impact on lifestyle. Treating physicians should question the need for long-term diuretics in these patients and use alternative agents where possible. In general, hypouricemic agents are underprescribed, and their use should be considered early in this group of high-risk patients," Dr. Stamp writes.

Loop diuretics associated with posttransplant gout risk

The investigators identified 47 living postrenal transplant patients with gout and matched each with a renal transplant recipient without gout. Cases and controls were matched for age, sex, and date of transplant; case notes were audited, and each patient was interviewed.

Patients with gout were more likely to be taking a loop diuretic (68% vs 34%, P <.001), to have posttransplant serum urate levels of .45 mmol/L or higher (64% vs 32%, P <.001), and to have higher serum creatinine and lower creatinine clearance. Pretransplant patients who subsequently developed gout had somewhat, but not significantly, higher serum urate levels.

Seventy percent of the posttransplant gout patients had repeated episodes, and more than half had gout attacks at least every 3 months with devastating effects on these patients' quality of life. Two thirds of the transplant recipients with gout were able to return to work after their renal transplants, but 48% subsequently required time off work because of their gout, and two thirds of this group lost more than 4 weeks of work.

Despite this outcome, only 17 of the 33 patients with repeated gout attacks were treated with a hypouricemic agent (16 with allopurinol, one with probenecid). Acute attacks of gout were treated with colchicine in 23/47 patients (49%), which resulted in diarrhea in 14/23 patients and colchicine myoneurotoxicity in one. Eight patients were treated with NSAIDs and 15 with corticosteroids.

Of the 16 patients treated with allopurinol, 11 had azathioprine replaced by mycophenylate mofetil and 3 had azathioprine discontinued, which was not replaced. No patients were treated with both allopurinol and azathioprine.

Earlier hypouricemic therapy recommended

"[A] case could be made in this high-risk population that hypouricemic therapy should be commenced after the first attack of gout given the high likelihood of recurrence," Dr. Stamp says.

Cyclosporine and diuretics have both been implicated in the development of gout in transplant recipients.² Loop and thiazide diuretics are thought to add to this problem by reducing renal excretion of uric acid and causing extracellular volume depletion.

"In the present transplant cohort, patients with gout were more likely to be taking a diuretic compared with those without gout. However, there was no association between serum uric acid concentration and diuretic use. Although the magnitude of the effect of diuretics on hyperuricemia and gout is difficult to quantify, it may be clinically important in this group of patients in whom therapeutic options are limited," the authors write.

References

1. Stamp L, Ha L, Searle M, et al. Gout in renal transplant recipients. Nephrology. 2006;11:367-371.
2. Abbott KC, Kimmel PL, Dharnidharka V, et al. New-onset gout after kidney transplantation: incidence, risk factors and implications. Transplantation. 2005;80:1383-1391.